Case report of acute encephalopathy caused by enterohemorrhagic Escherichia coli infection in a 24-year-old woman

2019 ◽  
Vol 59 (5) ◽  
pp. 274-278 ◽  
Author(s):  
Yuya Suzuki ◽  
Takao Fukushima ◽  
Takahiro Iwasawa ◽  
Gen Nakamura ◽  
Shigeki Nanasawa ◽  
...  
2020 ◽  
Vol 64 (4) ◽  
Author(s):  
Sabrina Mühlen ◽  
Isabell Ramming ◽  
Marina C. Pils ◽  
Martin Koeppel ◽  
Jana Glaser ◽  
...  

ABSTRACT Infections with enterohemorrhagic Escherichia coli (EHEC) cause disease ranging from mild diarrhea to hemolytic-uremic syndrome (HUS) and are the most common cause of renal failure in children in high-income countries. The severity of the disease derives from the release of Shiga toxins (Stx). The use of antibiotics to treat EHEC infections is generally avoided, as it can result in increased stx expression. Here, we systematically tested different classes of antibiotics and found that their influence on stx expression and release varies significantly. We assessed a selection of these antibiotics in vivo using the Citrobacter rodentium ϕstx2dact mouse model and show that stx2d-inducing antibiotics resulted in weight loss and kidney damage despite clearance of the infection. However, several non-Stx-inducing antibiotics cleared bacterial infection without causing Stx-mediated pathology. Our results suggest that these antibiotics might be useful in the treatment of EHEC-infected human patients and decrease the risk of HUS development.


2011 ◽  
Vol 79 (6) ◽  
pp. 2224-2233 ◽  
Author(s):  
Carla Calderon Toledo ◽  
Ida Arvidsson ◽  
Diana Karpman

ABSTRACTEnteropathogenicEscherichia coli(EPEC) and enterohemorrhagicE. coli(EHEC) are related attaching and effacing (A/E) pathogens. The genes responsible for the A/E pathology are carried on a chromosomal pathogenicity island termed the locus of enterocyte effacement (LEE). Both pathogens share a high degree of homology in the LEE and additional O islands. EHEC prevalence is much lower in areas where EPEC is endemic. This may be due to the development of antibodies against common EPEC and EHEC antigens. This study investigated the hypothesis that EPEC infections may protect against EHEC infections. We used a mouse model to inoculate BALB/c mice intragastrically, first with EPEC and then with EHEC (E. coliO157:H7). Four control groups received either a nonpathogenicE. coli(NPEC) strain followed by EHEC (NPEC/EHEC), phosphate-buffered saline (PBS) followed by EHEC (PBS/EHEC), EPEC/PBS, or PBS/PBS. Mice were monitored for weight loss and symptoms. EPEC colonized the intestine after challenge, and mice developed serum antibodies to intimin andE. colisecreted protein B (encoded in the LEE). Prechallenge with an EPEC strain had a protective effect after EHEC infection, as only a few mice developed mild symptoms, from which they recovered. These mice had an increase in body weight similar to that in control animals, and tissue morphology exhibited mild intestinal changes and normal renal histology. All mice that were not prechallenged with the EPEC strain developed mild to severe symptoms after EHEC infection, with weight loss as well as intestinal and renal histopathological changes. These data suggest that EPEC may protect against EHEC infection in this mouse model.


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